Anisperimus [LF 150195] is a deoxyspergualin analogue under development by Fournier Pharma (formerly Groupe Fournier) for the potential treatment of autoimmune disorders and transplant rejection. Anisperimus is a more potent, and less toxic analogue of 15-deoxyspergualin, an antibiotic used as an immunosuppressive agent to prevent rejection of organ transplants. Anisperimus enhances activation-induced T-cell death by facilitating caspase-8 and caspase-10 activation at the DISC level. Phase I clinical studies were being conducted by Fournier in France for Transplant rejection and Phase II clinical studies for Autoimmune disorders in Europe. However development of anisperimus has been discontinued.

Pirmagrel is the selective thromboxane synthetase inhibitor. The compound was well tolerated by all subjects without evidence of any adverse reactions. Serum thromboxane B2 levels (the stable metabolic product of thromboxane A2) were significantly reduced after administration of the compound, with the maximal effect of a 99 per cent reduction occurring at 0.5 and 1 hour after administration. Bleeding times showed a slight increase 2 hours after administration of the compound. Pirmagrel was able to completely prevent the increase in serum thromboxane B2 following allergen challenge in asthmatic patients; while it caused a very small reduction in the early response to allergen, there was no effect on the late response or on airway hyperresponsiveness. Pirmagrel was developed for the treatment of ischemic heart disorders and thrombosis. However, this development was discontinued.

Mifentidine, a histamine H2 receptor antagonist, was studied to treat the duodenal ulcer. This drug was in phase II clinical trials when apparently further researches had been discontinued.

Tecastemizole (aka Norastemizole) is an H1 receptor antagonist that showed great promise as potential next-generation antihistamine allergy medication. Sepracor developed Norastemizole through phase III clinical trials; however, the FDA rejected the application for approval on the grounds of an unacceptable profile of adverse side-effects including phospholipidosis and cardiomyopathies in animals exposed to the drug.

Oxisuran was developed by Parke-Davis as an antineoplastic agent. It was shown that this drug was a differential inhibitor of cell-mediated hypersensitivity. Experiments on rodents with experimental autoimmune encephalomyelitis have revealed that oxisuran was pharmacologically effective. However, information about the further development of the compound is not available.

Tiacrilast (also known as Ro 22-3747) is a quinazolinyl-propenoic acid derivative patented by Hoffmann-La Roche, Inc. as an antihypertensive useful for anaphylaxis management. Tiacrilast acts as a potent mast cell degranulation inhibitor in vitro and inhibits of antigen-induced histamine release from passively sensitized rat peritoneal cells in vitro. In preclinical models, Tiacrilast shows marked activity in rat passive cutaneous anaphylaxis assay, rat anaphylactic bronchospasm assay. In vitro studies have confirmed that the mechanism of action of Tiacrilast in the in vivo models is through allergic mediator release inhibition. Clinical evaluations of Tiacrilast in patients with ragweed sensitive allergic asthma, Tiacrilast demonstrates significant inhibitory activity relative to placebo in reducing acute airway responses to inhaled pollen extracts

Urocanic acid is a breakdown (deamination) product of histidine. In the liver, urocanic acid is an intermediate in the conversion of histidine to glutamic acid, whereas in the epidermis, it accumulates and may be both a UV protectant and an immunoregulator. Urocanic acid (UA) exists as a trans isomer (t-UA, approximately 30 mg/cm2) in the uppermost layer of the skin (stratum corneum). t-UA is formed as the cells of the second layer of skin become metabolically inactive. During this process, proteins and membranes degrade, histidine is released, and histidase (histidine ammonia lyase) catalyzes the deamination of histidine to form t-UA. t-UA accumulates in the epidermis until removal by either the monthly skin renewal cycle or sweat. Upon absorption of UV light, the naturally occurring t-UA isomerizes to its cis form, c-UA. Because DNA lesions (e. g. , pyrimidine dimers) in the lower epidermis can result from UV-B absorption, initial research proposed that t-UA acted as a natural sunscreen absorbing UV-B in the stratum corneum before the damaging rays could penetrate into lower epidermal zones. c-UA also suppresses contact hypersensitivity and delayed hypersensitivity, reduces the Langerhans cell count in the epidermis, prolongs skin-graft survival time, and affects natural killer cell activity. It has also been proposed that c-UA may mediate the transient alteration in immune surveillance resulting in immunosuppression induced after UV-irradiation, by interacting with immune cells locally and/or systemically to generate T cells with suppressor function.

Dinitrochlorobenzene (DNCB) is a chemical used in color photography processing. Dinitrochlorobenzene has been successfully used to treat warts. It requires follow-up applications that might be done either in the office by the doctor or a nurse, or at home by the patient. The therapy was working immunologically to enable the body to recognize the foreign virus. The cure is associated with normalization of the cell-mediated immune response. Some researchers and community activists proposed that when DNCB is applied to the skin once a week, it stimulates the immune system to control HIV replication and delay opportunistic infections. Some research shows that DNCB leads to increases in CD8 (T-killer or T-8) cells. Dinitrochlorobenzene is not approved by the FDA, and is considered experimental. There are possible drawbacks to this treatment. The autoeczematization is not rare. Dinitrochlorobenzene is used to induce experimental dermatitis in rats. It is a potent contact allergen.